Spondyloarthritis — overview

Last updated 28 Mar 2026 · Inflammatory Arthritis

Introduction

Spondyloarthritis (SpA) is a group of interrelated inflammatory arthritides characterised by involvement of the axial skeleton (sacroiliac joints and spine), peripheral joints (particularly hips and knees), and extra-articular manifestations (eye, skin, gastrointestinal, genitourinary involvement). The major subtypes include axial spondyloarthritis (axSpA), peripheral spondyloarthritis, psoriatic arthritis (PsA), reactive arthritis, and enteropathic arthritis (associated with inflammatory bowel disease).

Spondyloarthritis affects approximately 1–2% of the Australian population, with higher prevalence in males and typically age of onset 20–40 years. The condition is strongly associated with HLA-B27 positivity (up to 95% in axial disease). Early diagnosis and initiation of effective anti-inflammatory therapy, including NSAIDs, conventional DMARDs, and biologic agents (TNF inhibitors, IL-17 inhibitors), can significantly improve long-term outcomes and prevent progression of structural damage.

Pathophysiology and Classification

Genetic and Immunological Basis

Spondyloarthritis is a genetically predisposed, HLA-B27-associated inflammatory disorder. HLA-B27 positivity is present in 90–95% of patients with axial SpA but only 70% of patients with peripheral SpA and 40–60% in PsA. The exact mechanism involves aberrant presentation of arthritogenic antigens to T cells.

Major Subtypes and Classification

Axial spondyloarthritis (axSpA): Predominant inflammation of sacroiliac joints and/or spine. Includes ankylosing spondylitis (with definite radiographic changes) and non-radiographic axSpA. Most common form (60–70% of SpA).
Psoriatic arthritis (PsA): Associated with psoriasis. Peripheral predominant in 70% of cases; some have axial involvement.
Reactive arthritis: Follows gastrointestinal or genitourinary infection. Often transient; some progress to chronic arthritis.
Enteropathic arthritis: Associated with inflammatory bowel disease (Crohn's disease, ulcerative colitis). Peripheral and/or axial involvement.
Undifferentiated spondyloarthritis: Patients with SpA features not meeting criteria for specific subtype.

Clinical Presentation

Axial Spondyloarthritis

Onset: Typically 15–40 years old. Pain characteristics: Insidious-onset inflammatory back pain (pain worse in morning, improves with activity). Pain typically in buttocks and lower back. Stiffness: Morning stiffness lasting >30 minutes (often several hours). Stiffness improves with activity, not with rest.

Peripheral Arthritis Features

Peripheral joint involvement: Affects large joints (hips, knees, shoulders, ankles). Oligoarticular pattern (2–4 joints) is typical. Enthesitis: Inflammation at sites where tendons/ligaments attach to bone (Achilles insertion, plantar fascia, patellar tendon). Dactylitis: "Sausage-like" swelling of entire finger or toe.

Extra-Articular Manifestations

Ocular: Anterior uveitis (eye pain, photophobia, visual blurring) in 25–35% of patients. Skin: Psoriasis (in PsA), keratoderma blennorrhagicum (reactive arthritis), oral ulceration. Gastrointestinal: Increased frequency of inflammatory bowel disease association. Cardiac: Aortic regurgitation, conduction abnormalities (in advanced disease).

Investigations

Essential
HLA-B27 Testing
Positive in 90–95% of axial SpA, 70% of peripheral SpA, 40–60% PsA. Helpful for diagnostic confirmation. Negative result does not exclude diagnosis but makes axial disease less likely.
Essential
Inflammatory Markers (ESR, CRP)
Elevated in 50–70% of patients with active disease. Normal markers do not exclude diagnosis. Help assess disease activity and guide treatment response monitoring.
Essential
Imaging: X-rays (Sacroiliac Joints and Lumbar Spine)
Shows sacroiliitis (bilateral, symmetrical changes: sclerosis, erosion, fusion). Spine: syndesmophytes, ankylosis. Indicates ankylosing spondylitis (radiographic axSpA). Absence of changes does not exclude non-radiographic axSpA.
Available
MRI (Sacroiliac Joints and Spine)
More sensitive than X-rays for early inflammation. Shows bone marrow oedema, synovitis, and early structural changes. Useful in early disease diagnosis and non-radiographic axSpA.

Severity Assessment

MILD

Mild Inflammatory Activity

Limited peripheral joint involvement. Mild axial pain and stiffness. Normal/mildly elevated inflammatory markers. No structural progression on imaging. Good functional capacity.

Primary care; NSAIDs; monitoring for disease activity

MODERATE

Moderate Disease Activity

Multiple joint involvement or significant axial pain. Morning stiffness >1 hour. Elevated inflammatory markers. Early structural changes possible. Functional limitation present.

Rheumatology referral; NSAID optimisation; consider conventional DMARD or biologic agent

SEVERE

High Disease Activity with Damage

Multiple joints affected or significant axial involvement. High inflammatory markers. Progressive structural damage on imaging. Extra-articular manifestations. Significant functional impairment.

Specialist rheumatology; biologic therapy essential; consider combination therapy

Directed Therapy

First-Line: NSAIDs

NSAIDs are the foundation of SpA treatment, with evidence supporting both symptomatic benefit and potentially slowing radiographic progression in axSpA. High-dose, regular NSAIDs are recommended (not on-demand dosing).

💊

Indomethacin

Indocid® · NSAID

Adult Dose50–75 mg daily (in divided doses or extended-release 75 mg daily)

RouteOral

DurationOngoing; regularly review need

NotesTraditional first-line for axSpA. May slow radiographic progression. GI side effects common; use with gastroprotection (PPI). CNS side effects (headache, dizziness) possible.

PBS Status✓ PBS General Benefit

💊

Naproxen

Naprosyn® · NSAID

Adult Dose500–1000 mg daily (in divided doses)

RouteOral

FrequencyTwice daily

DurationOngoing; regularly review need

NotesAlternative to indomethacin. Long half-life allows twice-daily dosing. Similar efficacy. GI and cardiovascular side effects; use with gastroprotection.

PBS Status✓ PBS General Benefit

Second-Line: Conventional DMARDs

Conventional DMARDs have limited efficacy in axial SpA but are useful for peripheral joint involvement and PsA. Sulfasalazine (2–3 g daily in divided doses) is preferred for peripheral arthritis and enteropathic arthritis. Methotrexate (10–25 mg weekly) is used primarily in PsA and peripheral arthritis, particularly if skin involvement present.

Third-Line: Biologic Agents

TNF-alpha inhibitors: Adalimumab, etanercept, certolizumab, golimumab are highly effective for both axial and peripheral SpA. Reserved for patients with persistent disease activity despite NSAIDs and/or DMARDs. Require baseline TB screening, hepatitis B/C testing.

IL-17 inhibitors: Secukinumab, ixekizumab are effective for axial SpA and PsA. May be preferred first-line biologic for patients with concomitant psoriasis or TNF inhibitor intolerance.

Acute Management and Specialist Referral

Initial Presentation

When to suspect SpA: Young patient (15–40 years) with inflammatory back pain (morning stiffness >30 min, worse in morning, improves with activity). Peripheral arthritis (oligoarticular, affecting large joints). Enthesitis or dactylitis. Extra-articular features (uveitis, psoriasis, GI symptoms). HLA-B27 positivity. Family history of SpA.

Initial investigations: HLA-B27, ESR/CRP, X-rays of sacroiliac joints and lumbar spine. If early disease suspected and X-rays normal, MRI of sacroiliac joints and spine. Rheumatology referral recommended for all suspected SpA.

Acute Flares

Management: Optimise NSAID dosing (increase to maximum tolerated dose). Add short course of systemic corticosteroid (prednisolone 20–30 mg daily × 1–2 weeks, then taper) if significant functional impairment. Intra-articular corticosteroid injection for individual inflamed joints. Escalate biologic therapy if on inadequate dose or considering switch to alternative agent.

Monitoring and Follow-Up

Assessment of Disease Activity

Clinical assessment: BASDAI and ASDAS are validated tools to assess and monitor axial SpA activity. Inflammatory markers: ESR and CRP correlate imperfectly with disease activity; some patients have low markers despite active disease (MRI more sensitive). Imaging: Annual X-rays of sacroiliac joints and lumbar spine to assess progression.

Treatment Targets

Goal of therapy: Remission or low disease activity (ASDAS <2.1 or BASDAI <4). Most patients on combination therapy achieve this goal. Frequency of monitoring: Every 4–12 weeks initially; then every 3–6 months once stable. More frequent if considering medication changes or if extra-articular manifestations present.

Special Populations

👶 Juvenile-Onset SpA

Onset before age 16 yearsOften peripheral predominant; axial involvement develops later. NSAIDs first-line. DMARDs/biologics if inadequate response. Careful growth monitoring if on systemic corticosteroids.

Transition to adult careTransition planning from paediatric to adult rheumatology is important. Continue pharmacotherapy and disease monitoring seamlessly.

🤰 Pregnancy and Childbearing

NSAIDs safetyAvoid NSAIDs in third trimester. Paracetamol safe throughout pregnancy.

DMARDs and biologicsSulfasalazine, methotrexate, and TNF inhibitors have variable pregnancy safety. Discuss with rheumatologist regarding continuation during pregnancy and lactation.

Aboriginal and Torres Strait Islander Health Considerations

Spondyloarthritis prevalence in Aboriginal and Torres Strait Islander populations is not well-established but likely similar to other populations. However, diagnostic and treatment delays may occur due to limited rheumatology services in remote areas, potentially resulting in greater disease progression and functional impairment at time of diagnosis.

Diagnostic Delay

Limited access to HLA-B27 testing, imaging (X-rays, MRI), and rheumatology assessment in remote communities may delay diagnosis. Utilise clinical criteria and basic investigations available. Arrange specialist assessment via telehealth or patient transport. Early referral to regional rheumatology centre if SpA suspected.

Medication Access and Adherence

Access to NSAIDs and DMARDs may be limited. Biologic agents require specialist prescription and monitoring. Ensure access to PBS-funded medications. Establish shared-care arrangements between remote health centres and specialist rheumatology services.

Extra-Articular Manifestations Screening

Uveitis screening and ophthalmology access limited in remote areas. Educate patients on red flags (eye pain, photophobia). Arrange telehealth ophthalmology assessment if available. Rapid referral if uveitis suspected.

Comorbidities and Lifestyle Factors

Higher rates of smoking, obesity, and sedentary lifestyle in some communities increase SpA disease burden. Provide comprehensive health screening and comorbidity management. Exercise and lifestyle counselling adapted to local context and culture.

Stewardship and Key Points

Key Messages

Early diagnosis and treatment are critical: Delay in diagnosis results in more advanced disease at presentation and greater long-term morbidity. Suspicious clinical features should prompt HLA-B27 testing, imaging, and specialist referral.
NSAIDs are foundational therapy: Regular, high-dose NSAIDs (not on-demand) are essential. Evidence supports potential disease-modifying effect in axial SpA. Gastroprotection advised for long-term use.
Biologic therapy is highly effective: TNF inhibitors and IL-17 inhibitors dramatically improve disease activity and function. First-line biologic therapy recommended if inadequate response to NSAIDs.
Treat-to-target approach is optimal: Aim for remission or low disease activity (ASDAS <2.1 or BASDAI <4). Regular monitoring and treatment escalation needed to achieve target.
Extra-articular manifestations require coordinated care: Uveitis (ophthalmology), psoriasis (dermatology), IBD (gastroenterology). Screen for and manage these actively as part of comprehensive SpA care.

References

01
Sieper J, Deodhar A, Eric B, et al. Axial spondyloarthritis. Nat Rev Dis Primers. 2023;9(1):6.
02
van der Linden S, Valkenburg HA, de Jonge H. The risk of developing ankylosing spondylitis in HLA-B27 positive individuals: a family study approach. Arthritis Rheum. 1984;27(3):241-249.
03
Braun J, Baraliakos X, Listing J, et al. Persistent high rates of TNF-inhibitor therapy in ankylosing spondylitis. Rheumatology. 2011;50(11):2015-2019.
04
Australian and New Zealand Society for Rheumatology (ANZSRF). Evidence-based management of spondyloarthritis in Australia. 2024 Clinical Update.